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1 West Roxbury VA Medical Center and Harvard Medical School, West Roxbury, MA, USA
2 Department of Neurobiology, University of Massachusetts Medical School, Worcester, MA, USA
* To whom correspondence should be addressed. E-mail: pshiromani{at}hms.harvard.edu.
In mammals sleep is regulated by circadian and homeostatic mechanisms. The circadian component, residing in the suprachiasmatic nucleus (SCN), regulates the timing of sleep , whereas homeostatic factors determine the amount of sleep. It is believed that these two processes regulating sleep are independent since sleep amount is unchanged after SCN lesions. However, because such lesions necessarily damage neuronal connectivity, it is preferable to investigate this question in a genetic model that overcomes the confounding influence of circadian rhythmicity. Mice with disruption of both mPer 1 and mPer 2 have a robust diurnal sleep-wake rhythm in an entrained light-dark cycle but lose rhythmicity in a free-run condition. Here we examine the role of the mouse Period (mPer) genes on the rhythmic and homeostatic regulation of sleep. In entrained conditions, when averaged over the 24h period, there were no significant differences in waking, slow wave sleep (SWS) or REM sleep between mPer1, mPer2, mPer3, mPer1-mPer2 double mutants and wildtype (WT) mice. The mice were then kept awake for 6h (ZT 6-12) and the mPer mutants exhibited increased sleep drive indicating an intact sleep homeostatic response in the absence of the mPer genes. In free-run conditions (constant dark, DD), the mPer1-mPer2 double mutants became arrhythmic, but they continued to maintain their sleep levels even after 36d in free-running conditions. Although mPer1 and mPer2 represent key elements of the molecular clock in the SCN they are not required for homeostatic regulation of the daily amounts of waking, SWS or REM sleep.
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